We found that on many surfaces specific plasma proteins are absorbed rapidly out of blood. Subsequent interactions with the plasma follow; the resulting film determines the course of later events: . Factor XII may be adsorbed and activated to cause clotting, fibrinogen may be deposited to cause platelet adhesion, and gamma globulins may be deposited to cause granulocyte adhesion and spreading. However, the plasma if intact (not yet touched by glass-like surfaces) will "convert" fibrinogen on certain surfaces; platelets will not adhere to converted fibrinogen films. The substrate also determines what effect the globulins adsorbed on it will have on approaching granulocytes, e.g. on hydrophobic substrates, fibrinogen conversion is less and adsorbed globulin causes more deposition and spreading of granulocytes. We now propose to study effects of 1) flow and 2) flexing of substrate, applying only 1 of these events and during only 1 phase, namely while a) plasma is depositing proteins, b) plasma interacts with deposited proteins, or c) platelets and white cells are being, versus have been, exposed to plasma-treated substrate. Thus, conditions will resemble initial events on artificial heart, valve, vessel surfaces in vivo and on homodialyzer, oxygenator and accessory fabricated structure/blood surfaces ex vivo where we found that flow affects cell type adhering. Ellipsometry and other methods developed in our laboratory to detect and measure immune reactions at interfaces, will continue to be used to identify and quantitate proteins deposited and then affected by plasma. Adhesion and spreading of platelets and granulocytes, and their orientation, on the resulting surfaces as well as activity of clotting factors XII, kallikrein and XI will also be quantitated. Blood of species other than man will also be studied.